NADPH oxidase NOX4 is a glycolytic regulator through mROS-HIF1α axis in thyroid carcinomas
Abstract The function of the NAD(P)H oxidases (NOXs) family member NOX4 is to generate reactive oxygen species (ROS), however, the molecular function of NOX4 has not been fully studied and waiting to be clarified. To elucidate the function of endogenous Nox4 in human thyroid carcinomas, papillomatos...
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Nature Portfolio
2018
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oai:doaj.org-article:fefb3b60bdcf4c568ab5e80878a550a82021-12-02T15:07:59ZNADPH oxidase NOX4 is a glycolytic regulator through mROS-HIF1α axis in thyroid carcinomas10.1038/s41598-018-34154-82045-2322https://doaj.org/article/fefb3b60bdcf4c568ab5e80878a550a82018-10-01T00:00:00Zhttps://doi.org/10.1038/s41598-018-34154-8https://doaj.org/toc/2045-2322Abstract The function of the NAD(P)H oxidases (NOXs) family member NOX4 is to generate reactive oxygen species (ROS), however, the molecular function of NOX4 has not been fully studied and waiting to be clarified. To elucidate the function of endogenous Nox4 in human thyroid carcinomas, papillomatosis thyroid cancer cells were used to study the cell growth by knocking down the expression of NOX4 and knocking out its functional partner p22phox/CYBA. As a result, the increasement of mitochondrial ROS(mROS) was abolished due to both knockdown of NOX4 and p22phox knockout in hypoxia, which destabilized HIF1α decreasing glycolysis and retarded cell growth. These data suggests that Nox4 is potent oncotarget due to its role in regulating glycolysis through mROS-HIF1α pathway, thereby mediating proliferation in thyroid carcinomas.Ping TangHao DangJie HuangTao XuPing YuanJun HuJian-feng ShengNature PortfolioarticleP47phox KnockoutThyroid Cancer CellsExtracellular Acidification Rate (ECAR)NOX4 KnockdownPapillary Thyroid Cancer Cell LineMedicineRScienceQENScientific Reports, Vol 8, Iss 1, Pp 1-9 (2018) |
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P47phox Knockout Thyroid Cancer Cells Extracellular Acidification Rate (ECAR) NOX4 Knockdown Papillary Thyroid Cancer Cell Line Medicine R Science Q |
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P47phox Knockout Thyroid Cancer Cells Extracellular Acidification Rate (ECAR) NOX4 Knockdown Papillary Thyroid Cancer Cell Line Medicine R Science Q Ping Tang Hao Dang Jie Huang Tao Xu Ping Yuan Jun Hu Jian-feng Sheng NADPH oxidase NOX4 is a glycolytic regulator through mROS-HIF1α axis in thyroid carcinomas |
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Abstract The function of the NAD(P)H oxidases (NOXs) family member NOX4 is to generate reactive oxygen species (ROS), however, the molecular function of NOX4 has not been fully studied and waiting to be clarified. To elucidate the function of endogenous Nox4 in human thyroid carcinomas, papillomatosis thyroid cancer cells were used to study the cell growth by knocking down the expression of NOX4 and knocking out its functional partner p22phox/CYBA. As a result, the increasement of mitochondrial ROS(mROS) was abolished due to both knockdown of NOX4 and p22phox knockout in hypoxia, which destabilized HIF1α decreasing glycolysis and retarded cell growth. These data suggests that Nox4 is potent oncotarget due to its role in regulating glycolysis through mROS-HIF1α pathway, thereby mediating proliferation in thyroid carcinomas. |
format |
article |
author |
Ping Tang Hao Dang Jie Huang Tao Xu Ping Yuan Jun Hu Jian-feng Sheng |
author_facet |
Ping Tang Hao Dang Jie Huang Tao Xu Ping Yuan Jun Hu Jian-feng Sheng |
author_sort |
Ping Tang |
title |
NADPH oxidase NOX4 is a glycolytic regulator through mROS-HIF1α axis in thyroid carcinomas |
title_short |
NADPH oxidase NOX4 is a glycolytic regulator through mROS-HIF1α axis in thyroid carcinomas |
title_full |
NADPH oxidase NOX4 is a glycolytic regulator through mROS-HIF1α axis in thyroid carcinomas |
title_fullStr |
NADPH oxidase NOX4 is a glycolytic regulator through mROS-HIF1α axis in thyroid carcinomas |
title_full_unstemmed |
NADPH oxidase NOX4 is a glycolytic regulator through mROS-HIF1α axis in thyroid carcinomas |
title_sort |
nadph oxidase nox4 is a glycolytic regulator through mros-hif1α axis in thyroid carcinomas |
publisher |
Nature Portfolio |
publishDate |
2018 |
url |
https://doaj.org/article/fefb3b60bdcf4c568ab5e80878a550a8 |
work_keys_str_mv |
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